Brain, behavior, & immunity - health最新文献

{"title":"Immunological correlates of suicidality among adolescents with internalizing symptoms","authors":"","doi":"10.1016/j.bbih.2024.100866","DOIUrl":"10.1016/j.bbih.2024.100866","url":null,"abstract":"<div><h3>Background</h3><p>Suicide is a leading cause of death in adolescents and young adults globally. Well-established risk factors for suicide are depression and past suicide attempts. People experiencing suicidality may represent a distinct neurobiological group of people with depression. Because converging evidence has implicated inflammation in depression, we sought to investigate relationships between suicidality and immune markers in youth experiencing diverse mood and anxiety symptoms. We hypothesized that adolescents with suicidality would exhibit a unique immune signature.</p></div><div><h3>Methods</h3><p>Adolescents underwent semi-structured interviews and completed self-reported measures to assess psychopathology, including suicidality (suicidal ideation, plans, or attempts). Fasting blood samples were collected, cultured with and without lipopolysaccharide (LPS) to stimulate an inflammatory response, and analyzed for 41 immune analytes. To assess how immune function related to suicidality categorically and dimensionally, we conducted group comparisons and correlations while controlling for multiple comparisons using false discovery rate (FDR). To further uncover subtle immune-suicidality relationships, we employed a data-driven approach using factor analysis to extract major immune factors, each of which was subsequently correlated with suicidality measures.</p></div><div><h3>Results</h3><p>Among 126 participants, 29 were healthy controls and 97 participants had internalizing symptoms; within the clinical group, 57 experienced suicidality. Three immune analytes differed between healthy controls, suicidal, and non-suicidal adolescents with internalizing symptoms in the LPS condition: Flt-3L (<em>p</em>_<em>FDR</em> = 0.0246), GM-CSF (<em>p</em>_<em>FDR</em> = 0.0246), and IFN-γ (<em>p</em>_<em>FDR</em> = 0.0246). These analytes were negatively correlated with the Beck Scale for Suicide Ideation (BSSI): Flt-3L (ρ = −0.19, <em>p</em> = 0.04); GM-CSF (<em>ρ = −</em>0.26, <em>p</em> = 0.004); IFN-γ (<em>ρ =−</em>0.33, <em>p</em> = 0.0003). GM-CSF also negatively correlated with number of suicide attempts (ρ = −0.39, <em>p</em> = 0.003). Factor analysis reduced 41 analytes to several common immune factors across experimental conditions, with Flt-3L, GM-CSF, and IFN-γ all loading heavily onto immune factors that were hypoactive in suicidality. Through this data-driven approach, we detected further associations between suicidality and immune factors across all conditions.</p></div><div><h3>Conclusions</h3><p>Peripheral immune function may be distinctly altered in adolescent suicidality. Future work should examine immune-suicidality relationships longitudinally.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001443/pdfft?md5=a9cacdf9935f21ec312dfc2d13b4c6c5&pid=1-s2.0-S2666354624001443-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142270319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomics and psychotherapy: An integrative review","authors":"","doi":"10.1016/j.bbih.2024.100867","DOIUrl":"10.1016/j.bbih.2024.100867","url":null,"abstract":"<div><div>Gold-standard psychotherapies like cognitive-behavioral therapy (CBT) show beneficial effects, but patient responses vary, indicating a need to predict and optimize treatment efficacy. Gene expression analysis may offer insights into the interplay between psychosocial processes and biological factors that impact psychopathology and therapeutic response. This integrative review examines 17 studies that assess gene expression in the context of psychotherapy, highlighting innovative frameworks for incorporating gene expression analysis in diagnosis, predicting treatment response, and monitoring treatment progress. Current evidence points to transcriptional control pathways downstream of the hypothalamic-pituitary-adrenal (HPA)-axis and sympathetic nervous system (SNS) signaling pathways, particularly their effects on immune cells (e.g., pro-inflammatory processes and wound healing), as key areas for future research. Higher-level pathway analyses, whether theory-based or empirically driven, appear to offer the most robust framework for future studies. This review also discusses significant limitations of current literature and proposes directions for future research.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142419578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stressful life events across the lifespan and inflammation: An integrative data analysis","authors":"","doi":"10.1016/j.bbih.2024.100861","DOIUrl":"10.1016/j.bbih.2024.100861","url":null,"abstract":"<div><div>Experiencing more stressful life events has been linked to higher levels of inflammation, but this association may depend on when in the lifespan the stressors occur. To address this knowledge gap, we tested two lifespan theories, the accumulation of risks and sensitive period models, by assessing the association between the total number of stressful events and their life stage occurrence on later-life C-reactive protein (CRP). We harmonized data across two cohort studies, maximizing variation in stressors reported across the lifespan. Participants (N_total = 7,952, 57.7% female, M_age = 69) from the Health and Retirement Study (HRS: n = 5,136, M_age = 70.6) and the English Longitudinal Study of Aging (ELSA: n = 2,816, M_age = 66.1) completed retrospective surveys of stressful life events and indicated what year(s) each event occurred and had blood drawn ∼4.5 years later. Stressful events were summed across the participants’ lifespans (age 0 to current age) and within childhood (0–17 years), young adulthood (18–39), midlife (40–59), and late adulthood (60+). In main effects models, more cumulative stressors (γ = .05, SE = .02, p = .012) and stressors in young adulthood (γ = .06, SE = .03, p = .037) were associated with higher levels of CRP. In models with all life stages together among adults age 65+ (n = 4,972), experiencing more stressors in midlife significantly predicted higher levels of CRP (γ = .08, SE = .04, p = .038). Our findings replicate prior evidence of an association between cumulative stressors and inflammation and extend this work by identifying stressors in young adulthood and midlife as potentially unique sensitive periods that predict higher levels of later-life inflammation.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266635462400139X/pdfft?md5=e15f11392780bf40f29e0c3220402219&pid=1-s2.0-S266635462400139X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142316099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Executive deficits after SARS-CoV-2 infection: A cross-sectional population study","authors":"","doi":"10.1016/j.bbih.2024.100857","DOIUrl":"10.1016/j.bbih.2024.100857","url":null,"abstract":"<div><h3>Importance</h3><p>Despite the major implications of executive deficits in day-to-day functioning, few studies have investigated this in post-acute sequelae of SARS-CoV-2 infection using standardized measures that differentiate between aspects of executive function.</p></div><div><h3>Objective</h3><p>Examine whether SARS-CoV-2 infection is associated with deficits in executive functions and if so, investigate the duration of this association.</p></div><div><h3>Design, Setting, and Participants</h3><p>The present research has a cross-sectional design and uses data from the Norwegian Covid-19 Cohort study. The current cohort (<em>n</em> = 8102) completed the Behavior Rating Inventory of Executive Function- Adult Version (BRIEF-A) electronically between April 2021 and September 2021. During the assessment, 4183 of the included participants had a prior positive polymerase chain reaction test (PCR) for SARS-CoV-2 and 3919 were untested or had a confirmed negative PCR test.</p></div><div><h3>Exposure</h3><p>Laboratory-confirmed SARS-CoV-2 infection.</p></div><div><h3>Main outcomes and measures</h3><p>Executive functions were measured using the BRIEF-A, a self-report questionnaire comprising 75 items within nine theoretically and empirically distinct clinical scales. All participants self-reported on demographical variables and comorbidity. Information on sex and age was derived from the personal identification number, and vaccination status was obtained from the Norwegian Immunization Registry (SYSVAK).</p></div><div><h3>Results</h3><p>Participants with a positive SARS-CoV-2 status reported executive deficits in everyday life above the clinical threshold (T-score ≥65) more often than non-infected controls (383 vs. 225). Specifically, the SARS-CoV-2 positive status group indicated significantly more deficits related to metacognition, with the greatest difference demonstrated for working memory. This difference remained when adjusting for various demographic factors and comorbidities, with significantly greater odds of reporting above the clinical threshold following SARS-CoV-2 infection, as observed on the global executive composite score 6–12 months after infection (OR 1.97; 95% CI 1.51 to 2.55).</p></div><div><h3>Conclusions</h3><p>Our study confirms more perceived executive deficits following SARS-CoV-2 infection compared to non-infected controls, with metacognitive aspects being the most affected. These findings shed light on the potential functional difficulties that individuals may encounter during the post-acute phase of SARS-CoV-2 infection and may guide further development of targeted interventions addressing metacognitive domains of executive functioning.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001352/pdfft?md5=c79bf5ea7476c0f6b7a5e22bfc46fc30&pid=1-s2.0-S2666354624001352-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142228481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in S100 calcium-binding protein β (S100β) and cognitive function from pre- to post-chemotherapy among women with breast cancer","authors":"","doi":"10.1016/j.bbih.2024.100860","DOIUrl":"10.1016/j.bbih.2024.100860","url":null,"abstract":"<div><div>Many patients with cancer experience cancer-related cognitive decline (CRCD). Previous studies have shown that elevated S100β, a calcium-binding protein commonly found in glial cells, can exhibit neurotoxic effects, including disruption of the blood-brain barrier (BBB). We studied changes in S100β levels in patients with breast cancer receiving chemotherapy, and the relationship to changes in cognitive function. A total of 505 women with breast cancer (mean (sd) age; 53.4 (53.6)) and 336 age-matched controls without cancer (52.8 (10.3)) were included from a nationwide study as part of the National Cancer Institute Community Oncology Research Program (NCORP). Both groups provided blood samples and completed neurocognitive assessments within 7 days before the patients with breast cancer received their first chemotherapy dose (pre-chemotherapy; T1) and within 1 month of their last chemotherapy administration (post-chemotherapy; T2). Utilizing a linear mixed model, multivariate linear regressions, and Spearman rank correlations (r_s), we investigated longitudinal changes in serum S100β concentrations and their relationships to changes in neurocognitive outcomes over time. We observed an increase in S100β for patients with breast cancer (p = 0.002), but not for controls without cancer over time (p = 0.683). Additionally, we identified subtle relationships between increases in serum S100β and worsening in cognitive performance on the Backward Counting test (r_s = 0.11, p = 0.041) and self-reported FACT-Cog Perceived Cognitive Abilities (r_s = −0.10, p = 0.025). Regression analyses adjusted for age, race, body-mass index (BMI), education, menopausal status, anxiety, and depression revealed a trend remained for the relationship of S100β with Backward Counting. In conclusion, we found that patients with breast cancer experience a significant increase in concentration of serum S100β over the course of chemotherapy. This increase is correlated with worsening in some neurocognitive outcomes from pre-to post-chemotherapy, with trending results remaining following adjustment for covariates.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced heart rate variability is associated with altered clinical laboratory profile in people living with HIV","authors":"","doi":"10.1016/j.bbih.2024.100858","DOIUrl":"10.1016/j.bbih.2024.100858","url":null,"abstract":"<div><h3>Background</h3><p>We compared heart rate variability (HRV) indices between people living with HIV (PLWH) and HIV-negative individuals to ascertain the independent association between HIV infection and reduced HRV, and further investigated whether distinct clinical laboratory profiles exist between PLWH with and without reduced HRV.</p></div><div><h3>Methods</h3><p>This cross-sectional analysis included 304 PLWH and 147 HIV-negative individuals with comparable age and sex. Thirty-two routine clinical laboratory indices (including hematology and biochemistry) closest to the survey were extracted from the Electronic Medical Record System. HRV indices were divided into two categories: low (lowest quartile, Q1) and moderate-to-high (combined, Q2‒Q4).</p></div><div><h3>Results</h3><p>The time domain indices, ln(SDNN), ln(RMSSD), and ln(PNN50), as well as the frequency domain indices, ln(HF), ln(LF), and ln(VLF), were all significantly reduced in PLWH versus HIV-negative individuals (all <em>p</em> &lt; 0.05). These associations remained for ln(SDNN), ln(PNN50), ln(HF) and ln(LF) even after adjusting for potential confounders in multivariable models. PLWH with low HRV indices exhibited distinct clinical laboratory profiles that were characterized by an elevation in fasting plasma glucose, white blood cell count, neutrophil count, neutrophil%, and a reduction in albumin, total protein, urine creatinine, lymphocyte%, red blood cell count (RBC) and nadir CD4 count. The final stepwise logistic regression models for low SDNN included older age, decreased total cholesterol levels, elevated neutrophil count, and the use of antidiabetic medications, whereas the final model for low LF included older age, reduced RBC and the use of antidiabetic medications.</p></div><div><h3>Conclusion</h3><p>PLWH exhibit impaired parasympathetic activity, as evidenced by reduced SDNN, PNN50, LF and HF. Furthermore, PLWH who have reduced HRV indices exhibits distinct clinical laboratory profiles that are related to systematic inflammatory response and diabetes.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001364/pdfft?md5=6cb1526ada3dcb677cedc960a35a13b3&pid=1-s2.0-S2666354624001364-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142163021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pain research in a petri dish? Advantages and limitations of neuro-glial primary cell cultures from structures of the nociceptive system","authors":"","doi":"10.1016/j.bbih.2024.100854","DOIUrl":"10.1016/j.bbih.2024.100854","url":null,"abstract":"<div><p>How can we learn more about pain without causing pain in humans or animals? This short review focuses on neuro-glial primary cell cultures as models to study neuro-immune interactions in the context of pain and discusses their advantages and limitations.</p><p>The field of basic pain research places scientists in an ethical dilemma. We aim to understand underlying mechanisms of pain for an improved pain therapy for humans and animals. At the same time, this regularly includes the induction of pain in model animals. Within the field of psychoneuroimmunology, the examination of the complexity of neuro-immune interactions in health and disease as well as the bi-directional communication between the brain and the periphery make animal experiments an inevitable part of pain research. To address ethical and legal considerations as well as the growing societal awareness for animal welfare, scientists push for the identification and characterization of complementary methods to implement the 3R principle of Russel and Burch. As such, methods to <em>replace</em> animal studies, <em>reduce</em> the number of animals used, and <em>refine</em> experiments are tested. Neuro-glial primary cell cultures of structures of the nociceptive system, such as dorsal root ganglia (DRG) or the spinal dorsal horn (SDH) represent useful <em>in vitro</em> tools, when research comes to a cellular and molecular level. They allow for studying mechanisms of neuronal sensitization, glial cell activation, or the role of specific inflammatory mediators and intracellular signaling cascades involved in the development of inflammatory and neuropathic pain. Moreover, DRG/SDH-cultures provide the opportunity to test novel strategies for interventions, such as pharmaceuticals or cell-based therapies targeting neuroinflammatory processes. Thereby, <em>in vitro</em> models contribute to a better understanding of neuron-glia-immune communication in the context of pain and in the advancement of pain therapies. However, this can only be one piece in a large puzzle. Our knowledge about the complexity of pain will depend on studies in humans and animals applied <em>in vitro</em> and <em>in vivo</em> and will benefit from clear and open-minded interdisciplinary communication and transparency in public outreach.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001327/pdfft?md5=f1d81ae7b985b38adf98055c4683cce3&pid=1-s2.0-S2666354624001327-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142168038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dried bear bile exerts its antidepressant effect by modulating adrenal FXR to reduce peripheral glucocorticoid levels","authors":"","doi":"10.1016/j.bbih.2024.100856","DOIUrl":"10.1016/j.bbih.2024.100856","url":null,"abstract":"<div><p>Depression is a psychological disorder associated with prolonged stress, which involves abnormal activation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated levels of glucocorticoids (GC). Excessive GC can cause damage to the structure and function of the hippocampus, thereby triggering depressive symptoms. Studies suggest that the bile acid receptor farnesoid X receptor (FXR) may play a role in adrenal GC synthesis. This study aimed to explore the potential therapeutic effects of dried bear bile (DBB) on depression and its mechanism. We used the chronic unpredictable mild stress (CUMS) mouse model and FXR agonist GW4064 stimulated mice, as well as H295R human adrenal cortical carcinoma cells, employing behavioral tests, biochemical analysis, and gene expression analysis to assess the effects of DBB treatment on depressive behavior, serum corticosterone (CORT) levels, and adrenal FXR and steroid biosynthesis-related gene expression. The results showed that in both CUMS and GW4064-stimulated mice, DBB treatment significantly improved depressive-like behaviors and reversed serum CORT levels. Additionally, DBB suppressed the expression of steroidogenic regulatory genes in the adrenal glands of CUMS mice. In H295R cells, DBB treatment effectively reduced cortisol secretion induced by Forskolin, inhibited the expression of steroid biosynthesis-related genes, and suppressed cortisol production and HSD3B2 expression under conditions of FXR overexpression and FXR activation. Our findings suggest that DBB regulates adrenal FXR to modulate glucocorticoid synthesis and exerts antidepressant effects. DBB may serve as a potential therapeutic agent for depression by regulating GC levels and steroidogenesis pathway. Further research is underway to test the antidepressant effects of each DBB component to understand their specific contribution.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001340/pdfft?md5=44ec5973d9ccc3683359eca727b66317&pid=1-s2.0-S2666354624001340-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142151049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 receptors from the perspective of NLRP3 inflammasome pathway in depression: Potential role of cannabidiol","authors":"","doi":"10.1016/j.bbih.2024.100853","DOIUrl":"10.1016/j.bbih.2024.100853","url":null,"abstract":"<div><p>Many patients with depressive disorder do not respond to conventional antidepressant treatment. There is an ongoing interest in investigating potential mechanisms of treatment resistance in depression to provide alternative treatment options involving inflammatory mechanisms. Increasing evidence implicates the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome as a critical factor in neuroinflammation. ATP-induced P2X7 receptor (P2X7R) activation is a major trigger for inflammation, activating the canonical NLRP3 inflammatory cascade. Psychosocial stress, the primary environmental risk factor for depression, is associated with changes in ATP-mediated P2X7R signaling. Depression and stress response can be alleviated by Cannabidiol (CBD). CBD has an anti-inflammatory activity related to the regulation of NLRP3 inflammasome activation. However, CBD's effects on the inflammasome pathway are poorly understood in central nervous system (CNS) cells, including microglia, astrocytes, and neurons. This review will emphasize some findings for neuroinflammation and NLRP3 inflammasome pathway involvement in depression, particularly addressing the ATP-induced P2X7R activation. Moreover, we will underline evidence for the effect of CBD on depression and address its potential impacts on neuroinflammation through the NLRP3 inflammasome cascade.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001315/pdfft?md5=f4b20aca5fbbed4242d6de6fa00d0165&pid=1-s2.0-S2666354624001315-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142136083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic nasal inflammation early in life induces transient and long-term dysbiosis of gut microbiota in mice","authors":"","doi":"10.1016/j.bbih.2024.100848","DOIUrl":"10.1016/j.bbih.2024.100848","url":null,"abstract":"<div><p>The gut microbiota begins to colonize the host body following birth, develops during the suckling period and changes to the adult type after weaning. The early gut microbiota during the suckling period is thought to have profound effects on the host physiology throughout life but it is still unclear whether early dysbiosis is retained lifelong. Our previous study indicated that chronic nasal inflammation induces dysbiosis of gut microbiota in adult mice. In the present study, we addressed the question as to whether early exposure to chronic nasal inflammation induces dysbiosis, and if so, whether the dysbiosis is retained until adulthood and the sex differences in this effect. Male and female mice received repeated intranasal administration of lipopolysaccharide (LPS) or saline twice a week from P7 to P24 and were weaned at P24. The cecal contents were obtained for 16S rRNA analysis at 2 time points: at 4 weeks (wks), just after weaning, and at maturation to adulthood at 10 wks. The body weight did not differ between saline- and LPS-treated mice till around weaning, suggesting that the mothers’ milk was given similarly to all mice. At 4 wks, the beta diversity was significantly different between saline- and LPS-treated male and female mice and the composition of the gut microbiota changed in LPS-treated mice. The abundance of phylum Bacteroidota tended to decrease and that of Firmicutes increased in LPS-treated male mice, while the abundance of Deferribacterota increased in LPS-treated female mice. At 10 wks, the beta diversity was not different between saline- and LPS-treated mice, but the abundance of family Lachnospiraceae significantly decreased in LPS-treated male and female mice by LEfSe analysis. Together, chronic nasal inflammation early in life caused transient and long-term dysbiosis of gut microbiota, which may contribute to the onset and progress of metabolic and neuropsychiatric disorders.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624001261/pdfft?md5=eb72654fc47867a86e01c03d428ffb8e&pid=1-s2.0-S2666354624001261-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142097558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}